2021, Number 2
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Rev Cub Oftal 2021; 34 (2)
Involvement of reactive oxygen species in cataract formation
Molinet VLM, Pérez PAI, Morell OZ
Language: Spanish
References: 35
Page: 1-14
PDF size: 384.84 Kb.
ABSTRACT
Cataract comprises opacification of the crystalline lens, which may
progressively affect the cortex and the anterior subcapsular nucleus, secondary
to accumulation of damaged proteins on this level, with loss of balance between
production and elimination of free reactive oxygen species. The importance of
delaying or identifying specific markers, as well as promoting a new therapeutic
target, is the object of study and analysis of a variety of research lines. A review
was conducted of the literature published from 1 January to 20 July 2020. Use
was made of PubMed, Infomed, Clinical Key, Lilacs, EBSCO, SciELO, Prisma and
UpToDate metasearch engines in English and Spanish to identify new scientific
evidence about oxidative stress and its involvement in cataract formation. The
crystalline lens barrier serves as a medium for exchange between various
molecules, preventing entrance of antioxidants into the nucleus, which results
in opacification. Mitochondria on the crystalline lens cortex allow oxygen
removal. Oxidative phosphorylation then forms free superoxide radicals which
naturally accumulate on this level with the passing of time. With aging,
adaptive homeostasis loses its ability to respond to oxidative stress changes,
but the prophylactic, targeted use of antioxidants may change the ultimate fate
of this condition. Lack of balance in oxidation-reduction processes is the cause
of cataract formation.
REFERENCES
Davies JMS, Cillard J, Friguet B, Cadenas E, Cadet J, Cayce R, et al. TheOxygen Paradox, the French Paradox, and age-related diseases. GeroScience. 2017;39(5-6):499–550.
Yahelín FF, Gregorio MS, Damían LW, Nantembwa TC. Oxidative stress: itsimpact on cataracts. Rev Cubana Farm. 2009 [acceso: 12/02/2010];43(3).Disponible en: http://scielo.sld.cu/pdf/far/v43n3/far11309.pdf
Škiljić D, Nilsson S, Petersen A, Karlsson JO, Behndig A, Kalaboukhova L, etal. Oestradiol levels and superoxide dismutase activity in age-relatedcataract: a case–control study. BMC Ophthalmol. 2016;16(1):210.
Modenese A, Gobba F. Cataract frequency and subtypes involved in workersassessed for their solar radiation exposure: a systematic review. ActaOphthalmol. 2018;96:779–88.
Killian B, Yuan TH, Tsai CH, Chiu THT, Chen YH, Chan CC. Emission-relatedHeavy Metal Associated with Oxidative Stress in Children: Effect ofAntioxidant Intake. Internat J Environm Res Publ Health. 2020;17:3920.
Tsai CF, Wu JY, Hsu YW. Protective Effects of Rosmarinic Acid againstSelenite-Induced Cataract and Oxidative Damage in Rats. Internat J Med Sci.2019;16(5):729-40.
Sreelakshmi V, Abraham A. Protective effects of Cassia tora leaves inexperimental cataract by modulating intracellular communication, membraneco-transporters, energy metabolism and the ubiquitin-proteasome pathway.Pharmac Biol. 2017;55(1):1274-82.
Mustafa OM, Daoud YJ. Is Dietary Milk Intake Associated with CataractExtraction History in Older Adults? An Analysis from the US Population. JOphthalmol. 2020;2020:2562875.
Pedro Luis PG, José Luis A. Métodos para medir el daño oxidativo. RevCubana Med Mil. 2000 [acceso: 12/02/2010];29(3)9:192-8. Disponible en:http://scielo.sld.cu/scielo.php?script=sci_arttext&pid=S0138-65572000000300007
Truscott RJW, Friedrich MG. Molecular Processes Implicated in HumanAge-Related Nuclear Cataract. Invest Opthalmol Vis Sci. 2019;60:5007.
Kim EB, Kim HK, Hyon JY, Wee WR, Shin YJ. Oxidative Stress Levels inAqueous Humor from High Myopic Patients. Kor J Ophthalmol. 2016;30(3):172-9.
Nam SW, Lim DH, Cho KY, Kim HS, Kim K, Chung TY. Risk factors ofpresenile nuclear cataract in health screening study. BMC Ophthalmol.2018;18(1):308.
Höhn A, Weber D, Jung T, Ott C, Hugo M, Kochlik B, et al. Happily (n) everafter: Aging in the context of oxidative stress, proteostasis loss and cellularsenescence. Redox Biol. 2017;11:482–501.
Lu B, Christensen I, Ma L, Wang X, Jiang L, Wang C, et al. miR-24-p53pathway evoked by oxidative stress promotes lens epithelial cell apoptosis inage-related cataracts. Molec Med Rep. 2018;17(4):5021-8.
Zhang D, Li M. Puerarin prevents cataract development and progression indiabetic rats through Nrf2/HO 1 signaling. Molec Med Rep. 2019;20(2):1017-24.
Jie Xu, Dan Li, Tianyu Zheng, Yi Lu. Beta-amyloid expression in agerelatedcataract lens epithelia and effect of beta-amyloid on oxidativedamage in human lens epitelial cells. Molec Vis. 2017;23:1015-28.
Wert KJ, Velez G, Cross MR, Wagner BA, Teoh-Fitzgerald ML, Buettner GR,et al. Extracellular superoxide dismutase (SOD3) regulates oxidative stress atthe vitreorretinal interface. Free Rad Biol Med. 2018;124:408–19.
Zhang H, Davies KJA, Forman HJ. Oxidative stress response and Nrf2signaling in aging. Free Rad Biol Med. 2015;88:314–36.
Lim V, Schneider E, Wu H, Pang IH. Cataract Preventive Role of IsolatedPhytoconstituents: Findings from a Decade of Research. Nutrients.2018;10(11):1580.
Ullah R, Khan M, Shah SA, Saeed K, Kim MO. Natural AntioxidantAnthocyanins - A Hidden Therapeutic Candidate in Metabolic Disorders withMajor Focus in Neurodegeneration. Nutrients. 2019;11:1195.
Zhou J, Yao K, Zhang Y, Chen G, Lai K, Yin H, et al. Thioredoxin BindingProtein-2 Regulates Autophagy of Human Lens Epithelial Cells under OxidativeStress via Inhibition of Akt Phosphorylation. Oxid Med Cell Long. 2016;2016:1–17.
Batliwala S, Xavier C, Liu Y, Wu H, Pang IH. Involvement of Nrf2 in OcularDiseases. Oxidative Medicine and Cellular Longevity 2017;2017:1–18.
Wang X, Shen C, Zhu J, Shen G, Li Z, Dong J. Long Noncoding RNAs in theRegulation of Oxidative Stress. Oxid Med Cell Long. 2019;2019:1–7.
Heruye SH, Maffofou Nkenyi LN, Singh NU, Yalzadeh D, Ngele KK, Njie-Mbye YF, et al. Current Trends in the Pharmacotherapy of Cataracts.Pharmaceuticals. 2020;13(1):15.
Zhu J, Hou Q, Dong XD, Wang Z, Chen X, Zheng D, et al. Targeted Deletionof the Murine Lgr4 Gene Decreases Lens Epithelial Cell Resistance to OxidativeStress and Induces Age-Related Cataract Formation. 2015;10(3):e0119599.
Langford-Smith A, Tilakaratna V, Lythgoe PR, Clark SJ, Bishop PN, Day AJ.Age and Smoking Related Changes in Metal Ion Levels in Human Lens:Implications for Cataract Formation. 2016;11(1):e0147576.
Bennett TM, M’Hamdi O, Hejtmancik JF, Shiels A. Germ-line and somaticEPHA2 coding variants in lens aging and cataract. Plos One.2017;12(12):e0189881.
Wang F, Ma J, Han F, Guo X, Meng L, Sun Y, et al. DL-3-n-butylphthalidedelays the onset and progression of diabetic cataract by inhibiting oxidativestress in rat diabetic model. Scient Rep. 2016;6:19396.
Xingjun F, Sheng Z, Benlian W, Grant H, Binbin L, Jing Yang, et al.Evidence of highly conserved beta-crystallin disulfidome that can be mimickedby in vitro oxidation in age-related human cataractc and glutathione depletedmouse lens. Mol Cell Prot. 2015;14:3211-23. DOI:http://10.1074/mcp.M115.050948
Oladipo I, Awodele O, Oreagba I, Olayemi S, Iruegbukpe C, Balogun B, etal. Evaluation and comparison of the indices of systemic oxidative stress among black-africans with age-related cataracts or primary glaucoma. MiddEast Afr J Ophthalmol. 2015;22(4):489-94.
Saraf S, Dubey S, Saha S, Kaithwas G. Effect of standardized fruit extractof Luffa cylindrica on oxidative stress markers in hydrogen peroxide inducedcataract. Ind J Pharmacol. 2015;47(6):644-8.
Wei Z, Caty J, Whitson J, Zhang AD, Srinivasagan R, Kavanagh TJ, et al.Reduced Glutathione Level Promotes Epithelial-Mesenchymal Transition inLens Epithelial Cells via a Wnt/β-Catenin–Mediated Pathway. Am J Pathol.2017;187:2399–412.
Shi W, Riquelme MA, Gu S, Jiang JX. Connexin hemichannels mediateglutathione transport and protect lens fiber cells from oxidative stress. J CellSci. 2018;131(6):212506.
Maddirala Y, Tobwala S, Karacal H, Ercal N. Prevention and reversal ofselenite-induced cataracts by N-acetylcysteine amide in Wistar rats. BMCOphthalmol. 2017 26;17(1):54.
Wu C, Liu Z, Ma L, Pei C, Qin L, Gao N, et al. MiRNAs regulate oxidativestress related genes via binding to the 3′ UTR and TATA-box regions: a newhypothesis for cataract pathogenesis. BMC Ophthalmol. 2017;17(1):142.